INTRODUCTION: Barrett's esophagus (BE) is the result of continuous injury of the esophageal mucosa by gastric refluxate. This condition can progress to low-grade (LGD) and high-grade dysplasia (HGD) and eventually to adenocarcinoma. While excellent results are reported in terms of reflux and symptom control in patients with BE undergoing antireflux surgery (ARS), the impact of a fundoplication on progression and regression of dysplasia is debated. The aim of this article is to review the effects of ARS on regression and progression of LGD to HGD or cancer in patients with dysplastic BE. MATERIALS AND METHODS: A review of the literature in PubMed/Medline electronic databases has been performed. RESULTS: ARS might decrease but not eliminate the risk of progression to dysplasia or cancer in BE patients. ARS may promote regression of dysplastic BE only in short-segment BE, but not in long-segment BE. Modulation of gene expression is involved in the genesis and reversion of short-segment intestinal metaplasia after ARS. CONCLUSIONS: Close and long-term surveillance by 24-hour pH monitoring and upper endoscopy is recommended in BE patients who undergo ARS to identify postoperative pathological reflux, and to early detect dysplasia or even adenocarcinoma. Further studies are requested to assess the molecular effects of ARS in dysplastic BE.
INTRODUCTION: Barrett's esophagus (BE) is the result of continuous injury of the esophageal mucosa by gastric refluxate. This condition can progress to low-grade (LGD) and high-grade dysplasia (HGD) and eventually to adenocarcinoma. While excellent results are reported in terms of reflux and symptom control in patients with BE undergoing antireflux surgery (ARS), the impact of a fundoplication on progression and regression of dysplasia is debated. The aim of this article is to review the effects of ARS on regression and progression of LGD to HGD or cancer in patients with dysplastic BE. MATERIALS AND METHODS: A review of the literature in PubMed/Medline electronic databases has been performed. RESULTS: ARS might decrease but not eliminate the risk of progression to dysplasia or cancer in BE patients. ARS may promote regression of dysplastic BE only in short-segment BE, but not in long-segment BE. Modulation of gene expression is involved in the genesis and reversion of short-segment intestinal metaplasia after ARS. CONCLUSIONS: Close and long-term surveillance by 24-hour pH monitoring and upper endoscopy is recommended in BE patients who undergo ARS to identify postoperative pathological reflux, and to early detect dysplasia or even adenocarcinoma. Further studies are requested to assess the molecular effects of ARS in dysplastic BE.
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